Among the various theories attempting to explain the aging process, the free radical theory of aging has received increased recognition over the past four decades (Harman, 1956; Sohal and Weindruch, 1996). A basic tenet of this theory is that reactive oxygen species (ROS) are produced as a normal byproduct of aerobic life and that accumulation of oxidative damage caused by ROS underlies the fundamental changes found in senescence. At least three lines of evidence support the theory, (a) Aging has been shown to correlate with the production of ROS and the capacity of cellular antioxidant defense systems (Harman, 1956; Ames et al., 1993; Yu, 1994). (b) An increasing number of age-related and degenerative diseases have been found to have an etiological component associated with ROS generation (Ames et al., 1993) and (c) strategies that are effective to reduce oxidative stress are also found to affect aging. A clear example is dietary or caloric restriction in rodents (Sohal and Weindruch, 1996).
Research over the past two decades has shown that ROS generation is a major cause of cell and tissue injury associated with rigorous physical exertion (Jenkins, 1993; Meydani and Evans, 1993). ROS resulting either from increased oxygen consumption or from specific pathways activated during or after exercise can elicit a series of biochemical modifications to the various cellular components causing a more oxidized environment within the cell generally termed "oxidative stress". However, physical exercise is an intimate part of the life cycle as organisms need the mobility to pursue food, escape predators, and ensure reproduction. The most prominent biological change occurring during exercise is the increased metabolic rate, matched by an enhanced rate of mitochondrial respiration and oxidative phosphorylation. It is estimated that during maximal muscular contraction in men oxygen consumption at the local muscle fibers can reach as high as 100 fold of the resting levels, while the whole body oxygen consumption increases by -20 fold (Jenkins, 1993). Such a high rate of oxygen flux may provoke increased electron "leakage" to molecular oxygen to form superoxide radicals (O2* ), above those found at the resting condition. Thus exercise imposes an oxidative stress in the vicinity of the mitochondria and other critical organelles essential for cell life (Yu, 1994).
In this chapter we choose to focus on the skeletal muscle for the following three reasons, (a) The general topic of aging and oxidative stress has been reviewed previously by many experts in the field, (b) Deterioration of skeletal muscle function is an important issue in medical gerontology because of the critical role of muscle for mobility and normal life, (c) Skeletal muscle has displayed some unique characteristics during aging both in terms of free radical production and antioxidant systems. It is important to keep in mind that the extent of cell oxidative damage is determined by the rate of not only ROS production, but also ROS removal provided by the antioxidant defense systems (including the capacity to repair the damage). Thus, age-related changes in muscle antioxidant capacity and possible influences of physical exercise will be emphasized.
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